Heart failure for nurses. Second year nsg students.

1. HEART FAILURE
By: Saili Gaude
Asst. Prof.
Medical Surgical Nursing

2. DEFINITION
▪ Heart failure is a physiologic state in which
the heart cannot pump enough blood to meet
the metabolic demands o the body.

3. Clinical Syndrome
▪ Volume overload
▪ Inadequate tissue perfusion
▪ Poor exercise tolerance

4. Etiology /Risk Factors
▪ Any condition that
weakens the heart muscles
can cause heart to fail !!!

5. Intrinsic vs Extrinsic factors
EXTRINSIC
FACTORS
INTRINSIC
FACTORS
Factors
originating
from within
the heart
Excessive
factors that
place high
demands on
heart
Pre-load After-load

6. Intrinsic Factors
▪ Coronary artery disease
▪ Cardiomyopathy
▪ Dysrhythmias
▪ Valvular disease
▪ Constrictive pericarditis
▪ Cardiac tamponade

7. Extrinsic Factors
Pre-load
▪ Initial stretching
of the heart
muscles before
contraction
Afterload
▪ It is the pressure
against which the
heart must work to
eject blood during
systole.

8. Conditions that increases
preload
▪ Mitral or tricuspid regurgitation
▪ Hypervolemia
▪ Congenital defects
▪ Ventricular septal defects
▪ Patent ductus arteriosus

9. Conditions that
increases after load
▪ Hypertension
▪ Aortic or pulmonary stenosis
▪ High peripheral vascular resistance

10. Pathophysiology-
compensated HF
▪ Ventricular dilatation
▪ Increased sympathetic nervous system
stimulation
▪ Stimulation of renin angiotensin system

11. Ventricular dilation
▪ Lengthening of muscle fibres that increases
the volume in the heart chambers.
▪ Frank starlings mechanism : Increased filling
volume dilate the ventricle Increases the
contractility

12. Increased sympathetic nervous
system stimulation

13. Renin Angiotensin
System
▪ Vasoconstriction
▪ Retention of sodium and water
▪ Plasma volume expansion
▪ Increase in preload

15. Decompensated heart
failure
 Remodelling
Sustained Neurohormonal Activation

16. Remodelling
▪ Remodeling is thought to result from
hypertrophy of the myocardial cells and
sustained activation of neurohormonal
compensatory systems.
▪ To reduce wall stress during ventricular
dilation the myocardial cells hypertrophy
(Laplace Law).
▪ Prolonged dilation causes permanent changes
leading to further deterioration of the heart
failure.

17. Sustained neurohormonal
activation
▪ Wall stress stimulates neurohormonal
activity.long term activation causes a toxic
effect on the heart that promotes myocytes
hypertrophy and myocardial fibrosis.

18. Types of
heart
failure

19. LVF vs RVF
Backward vs Forward
heart failure
High output vs low
output failure

21. Theory
▪ “The theory behind the left versus right
ventricular failure is based on the fact
that fluid accumulates behind the
chamber that fails first.”

22. Ventricular
interdependence
▪ Because the circulatory system is a
closed circuit , impairments of one
ventricle commonly progresses to failure
of the other.
▪ This is called as ventricular
interdependence.

23. Left ventricular failure
▪ As the ability to pump blood forward from the
left side of the heart is decreased, the
remainder of the body, does not receive
enough oxygen especially when exercising,
resulting in fatigue.
▪ Congestion of pulmonary vasculature with
symptoms being predominantly respiratory in
nature.

24. Clinical manifestations
▪ Dyspnea
▪ Orthopnea
▪ Paroxysmal nocturnal dyspnea
▪ Cheyne stokes respiration.
▪ Frothy or blood tinged hacking cough
▪ Bilateral crackles
▪ Gallop

25. ▪ Pulsus alternans
▪ Cerebral hypoxia
▪ Fatigue and muscle weakness
▪ Nocturia
Clinical manifestations
(Cont)

26. Complications of LVF
▪ PULMONARY EDEMA
•Medical emergency
•Fluid accumulates within the
alveoli, bronchioles and
bronchi due to increased
capillary pressure within the
lungs.

27. Right Ventricular failure
▪ Inability of the right
ventricle to pump
adequate amount of
blood leading to
systemic venous
congestion, therefore
peripheral edema and
hepatic congestion and
tenderness.

28. Clinical manifestations
▪ Hepatomegaly – enlargement of liver;
occurs due to venous congestion of the liver.
▪ Cardiac cirrhosis- the venous congestion
of the liver causes anoxia of parts of the liver
which later becomes necrotic. This areas can
later turn fibrotic or sclerotic and is called
cardiac cirrhosis of liver.

29. Clinical manifestations
(Cont)
▪ Cardiac cachexia : increased workload of
heart and extreme work of breathing increases
metabolic demand while abdominal venous
congestion causes anorexia, nausea and
bloating.
▪ The combination of both leads to marked
wasting of tissue mass called as cardiac
cachexia.

30. Clinical manifestations
(Cont)
▪ Dependent edema: early manifestation
of RVF. Venous congestion in the peripheral
vascular bed causes the fluid shifts out of
capillary beds into the interstitial space.
▪ Anasarca : a late manifestations
;substantial and generalized edema.

31. 2. Backward failure
vs
Forward failure

32. Backward failure
▪ Ventricle’s inability to eject
completely,
▪ Increases ventricular filling
pressures, causing venous and
pulmonary congestion.

33. Forward failure
▪ Inadequate perfusion.
▪ Decreased contractility reduces stroke
volume and cardiac output, diminishing
blood supply to vital organs.
▪ Causes mental confusion, muscle
weakness and renal retention of
sodium and water.

34. 3. High Output failure
vs
Low Output failure

35. High output failure
▪ Occurs when high or
normal output levels
cannot meet increased
demands of the body.

36. Low output failure
▪ Poor ventricular pumping
action and a low output
causes hypoperfusion of
organs thus not meeting
their demands.

37. 4. Decompensated
failure
vs
Chronic Heart failure

38. Decompensated
▪ Acute and unstable
▪ Heart cannot
compensate for the
demands.
Chronic heart failure
▪ Stable and long term
▪ Heart manages to
compensate for the
demands.

39. Diagnosis
1. The Framingham criteria
2. BNP
3. ECG
4. Chest Xray
5. Echocardiogram

40. 1.FRAMINGHAM
CRITERIA
Presence of any 2 major or 1 major and
2 minor criteria

41. Major criteria
▪ S3 heart sound present (‘gallop’ sound)
▪ Acute pulmonary oedema (left side of heart is unable to
clear fluid from lungs)
▪ Weight loss of more than 4.5kg in 5 days when treated
(patients lose their retained fluids)
▪ Paroxysmal nocturnal dyspnoea
▪ Abdominojugular reflux (JVP waveform rises when
pressure applied over liver area)
▪ Neck vein distended (i.e. JVP elevated at rest)
▪ Increased cardiac shadow on X-ray (cardiomegaly: heart
occupies more than ≈50% of chest diameter)
▪ Crackles heard in lungs

42. Minor
▪ Hepatomegaly
▪ Effusion, pleural
▪ Ankle oedema bilaterally
▪ exeRtional dyspnoea
▪ Tachycardia
▪ Vital capacity decreased by a third of
maximum value
▪ Nocturnal cough

43. 2.BNP
B-type natriuretic peptide is a protein
secreted from the ventricles in response to
overload .

44. >2,000 – require urgent
referral to cardiology for an
echocardiogram (<2 weeks)
400 – 2,000 – require
referral to cardiology for an
echocardiogram (<6 weeks)
<400 – heart failure is
unlikely and consider an
alternative diagnosis
BNP Values

45. 3.ECG
Measures the electrical activity of the heart
as it contracts.

46. ECG
▪ Performed on all suspected cases of heart
failure.
▪ May indicate the underlying cause of heart
failure.
▪ A normal ECG makes heart failure unlikely
(89% sensitivity).

47. 4.Chest Xray
Uses a small amount of radiation to create
pictures of the structures in and around
the chest.

48. ▪ Shows signs of
pulmonary congestion
and rule out any other
alternative diagnosis.
▪ A normal CXR does
not exclude the
possibility of a heart
failure.

49. 5.Echocardiogram
A probe sends out and records sound waves
of the heart to produce moving image of the
heart on a computer.

50. ▪ Recommended
test
▪ Can confirm
diagnosis
▪ Calculates cardiac
kinetics.
▪ Helps to stratify the
type of Heart
failure.

51. Medical Management

52. Reduce myocardial
workload
▪ Diuretics
▪ Vasodilators – nitroglycerine
▪ Morphine
▪ Beta adrenergic antagonist

53. Elevation of client’s head
▪ Placed high fowler’s to reduce
pulmonary congestion and reduce
dyspnea.
▪ Leg elevation is contraindicated as
it increases venous return.

54. Reduce fluid retention
▪ Sodium restricted diet- 2-4g sodium
recommended.
▪ In case of severe heart failure, fluid is
restricted to 1000 ml/day.

55. Improve ventricular
pump performance.
1. Dobutamine
2. Dopamine
3. Milrinone

56. Dobutamine
▪ Produces strong beta stimulatory effects
within the myocardium , increasing heart rate,
AV conduction and myocardial contractility..
▪ Capable of increasing cardiac output without
increasing myocardial oxygen demands.

57. Dopamine
▪ Catecholamine with alpha, beta and dopa
adrenergic activities.
▪ Increases GFR and helps in excretion of
sodium.

58. Milrinone
▪ Inotropic agent that dilated the pulmonary
vasculature.

59. Supplement oxygen
▪ Partial or non rebreathing mask
to provide high concentrations
of oxygen.
▪ Intubation with ventilatory
support in case the paO2 does
not reach above 60mmHg.
▪ Bronchodilators in case of
severe bronchospasm or
constriction.

60. Control dysrhythmias
▪ Atrial fibrillation is commonest.
▪ Can lead to embolic stroke thus controlled by
anticoagulant therapy.
▪ Arrhythmia controlled by amiodrone.

61. Reduce myocardial
remodelling
▪ ACE inhibitors:
▪ Reduces remodelling changes in the heart.
▪ Reduces afterload , increases renal blood flow
and enhances diuresis.

62. Reduce stress and risk of
injury
▪ Rest
▪ Reduce anxiety
▪ Tranquilizers, and barbiturates.

64. Ventricular assist devices
▪ Mechanical pump that’s used to support heart
function and blood flow in a weakened heart.
▪ Types: transcutaneous vs implantable

65. Implantable VAD

66. Transcutaneous VAD

68. Heart transplant
▪ In severe heart failure, with irreversible
damage to the heart .
▪ Types :
orthotopic heart transplant : removal of
diseased heart and replacing it with the
donors heart.
▪ Heterotopic heart transplant : when the
donor’s heart is sutured onto the diseased
portion of the heart.

69. Orthotopic heart
transplant
Heterotopic heart
transplant

70. Cardiomyoplasty
▪ Involves wrapping the latissimus dorsi muscle
around the heart and electro stimulating it in
synchrony with the ventricular systole.
▪ Patients with low cardiac output, but not a
candidate of heart transplant.

71. Cardiomyoplasty

72. Digoxin therapy for
chronic heart failure
▪ A positive ionotrope
▪ Slows and strengthens the heart beat .
▪ Improved cardiac output enhances kidney
perfusion , which may create a mild diuresis of
sodium and water.
▪ Toxicity- plasma levels more than 2mcg/L

73. Nursing diagnosis
▪ Decreased cardiac output related to heart
failure.
▪ Excess fluid volume related to reduced
glomerular filtration rate.
▪ Impaired gas exchange related to fluid in
alveoli.
▪ Ineffective tissue perfusion related to
decreased cardiac output.

74. ▪ Risk for activity intolerance related to
decreased cardiac output.
▪ Risk for impaired skin integrity related to
decreased tissue perfusion and activities.
▪ Risk for anxiety related to decreased cardiac
output.